The invention relates to complexing cresolase with copper chelating agents and includes the said complexes and a method for their preparation. It also includes a method of inhibiting L 1210 mouse leukemia using said complexes.
The tyrosinase gene is expressed only in mesenchymal melanocytes, functioning in mammals as dopa oxidase or catecholase. In other germ layers, tyrosinase exists at ribosomal membrane sites in blocked form, capable of release under conditions of tissue dissociation. This blocked tyrosinase (hereinafter called TYBLOC) functions as cresolase.
My theory of "binary sequencing" operationally defines TYBLOC by virtue of its effect on proline hydroxylase, as inhibitory to mesenchymal stem cell .alpha., .alpha. or non-differential division. TYBLOC therefore herein represents a naturally-occuring regulatory molecule Which serves as the first line of defense of mesenchymal mitotic activity.
Such mitotic inhibition is imitated by complexes of cresolase-active tyrosinase and copper chelating agents. Raw material is brown (Type I) common edible mushroom. A production protocol for this TYBLOC complex is detailed herein.
The theory of binary sequencing began with the observation that cancer and mesenchyme are operationally equivalent. A subsequent article classified mesenchyme as the identity element of the mathematical group S.sub.3. TYBLOC was found to satisfy the mathematical requirements for Z.sub.2 of the group S.sub.3 and its mode of action detailed.
Theoretically TYBLOC has the following functions:
1. as a frameshift doubler of quanine-cytosine residues in procollagen. PA1 2. as a block to .alpha.,.alpha. stem cell non-differential division. PA1 1. heat stable PA1 2. dialysable PA1 3. exhibits no sulfhydryl properties PA1 4. substantially inactivated by U.V. irradiation.
The latter action is of interest, insofar as anti-carcinogenic activity is concerned. Its proposed mechanism is as follows:
TYBLOC complex is a blood-borne membrane-specific cresolase isoenzyme which carries a copper chelator to proline hydroxylase at the microsomes. Both tyrosinase and proline hydroxylase are copper-containing enzymes synthesized at ribosomal sites.
Proline bydroxylase, characteristic only of mechenchyme, was proposed as the cell-divisional initiator protein. By sharing the copper chelator of the TYBLOC complex, the action of proline in electronic oxidation is curbed, effectively switching off cell division. The balanced steady-state between differential and non-differential cell division is thereby maintained, and the switched-off cell differentiates.
On this view based entirely of applicant's theory and tests on mouse leukemia cancer represents a biochemical lesion in TYBLOC from "whatever" cause. Intravascular administration of TYBLOC complex serves as effective replacement therapy.
In electronic terms, TYBLOC represents a "load" upon current generated by the electronic oxidation activity of proline hydroxylase, a proposed enzymatic cell-divisional "trigger". A break in the TYBLOC according to applicant's theory leads to cancer by creating an electrical "short" in the proline hydroxylase oxidative system. Current diversion into this oxidative and mitotic pathway according to applicant's theory and tests on mouse leukemia results in cancer, whereby the steady-state between differential and non-differential cell division is distorted.
While I believe the above disclosed theory and mechanism are correct, it will be understood that my invention is not limited thereby.